To evaluate the effects of early regular exercise and to assess the electrophysiological and histopathological findings of the rat tail nerve in relation to the timing of exercise training for swimming exercise in rats with diabetic neuropathy.
We used 70 Sprague-Dawley male rats, and the experimental group comprised 60 rats, and the control group comprised 10 rats. Diabetes was induced by intraperitoneal injection of streptozotocin. Blood glucose concentrations were measured in tail vein blood samples. The experimental group was divided into 6 subgroups according to insulin treatment and swimming exercise: group 1, diabetic control; group 2, insulin treated; group 3, insulin untreated with early swimming exercise; group 4, insulin treated and early swimming exercise; group 5, insulin treated and late swimming exercise; and group 6, insulin untreated with late swimming exercise. Sensory and motor nerve conduction studies were performed weekly up to the 13th week using rat tail nerves. The effect on structural diabetic neuropathy was assessed by morphometry and ultrastructural examination of the rat tail nerve fiber at the 14th week.
An exercise effect was observed in the insulin treated groups, but it was not observed in the insulin untreated groups. The sensory nerve conduction study in the rat tail revealed significantly prolonged latency and decreased amplitude in groups 1 and 6, and a further delay was observed in group 5 when compared to group 4. Decreased thickness of myelin was found in groups 1 and 6 through morphometry.
Early regular exercise programs in addition to conventional insulin treatment may retard the progression of diabetic peripheral neuropathy.
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Objective: The purpose of this study is to prove protective action of melatonin on the development of neuropathy in diabetic rat.
Method: The experimental rats (Sprague-Dawley) were divided into 3 groups: Group 1, streptozotocin-induced diabetic rats with trial of melatonin; Group 2, streptozotocin-induced diabetic rats without trial of melatonin; Group 3, normal control. Streptozotocin was injected intraperitoneally in group 1 and 2. Melatonin was administered per orally in group 1 from 1 week after the injection of streptozotocin. The melatonin effect on diabetic neuropathy was evaluated by the measurement of conduction velocities and amplitudes of rat tail mixed nerve action potentials. The electrophysiologic examinations were performed before and 2, 4, and 6 weeks after administration of streptozotocin.
Results: The rat tail mixed nerve conduction velocities were decreased at 4 weeks in group 1 and 2, and showed significant improvement at 6 weeks in group 1 as compared with those of group 2 (p＜0.05). The amplitudes of the compound nerve action potentials did not show difference before and after streptozotocin and melatonin trials, neither among groups.
Conclusion: In this experimental study, we observed the inhibitory effect of melatonin on the progression of polyneuropathy in early stage of diabetic rat. For the clinical application to human beings, further study is required.
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